1. NAME1.1 Scientific NameAtrax robustusAtrax spp. (2 undescribed species)
Hadronyche adelaidensisHadronyche cerbereaHadronyche eyreiHadronyche flindersiHadronyche formidabilisHadronyche infensaHadronyche meridianaHadronyche modestaHadronyche pulvinatorHadronyche validaHadronyche venenataHadronyche versutaHadronyche spp. (at least 20 undescribed species)
(Gray 1988)
1.2 FamilyHexathelidae (Note: previously placed in Dipluridae)
Sub-family: Atracinae1.3 Common NamesFunnel web spiders (whole group)
Atrax robustus Sydney funnel web spiderHadronyche formidabilis Northern tree funnel web spiderHadronyche cerberea Southern tree funnel web spiderHadronyche versuta Blue mountains funnel web spider2. SUMMARY2.1 Main risks and target organsWhile the majority of funnel web spider bites, even by the proven
lethal Atrax robustus, are minor and without systemic
envenomation, when severe effects do occur they may prove
difficult to treat and end fatally. Antivenom has had a
significant effect in reducing the likelihood of fatal outcome.
Only Atrax robustus is a proven cause of fatalities. It is now
established that Hadronyche formidabilis, H. infensa, H. versuta,
H cerberea, Hadronyche spp.7 can cause dangerous bites in man.
For most other Hadronyche spp there is no present evidence that
they are dangerous to man, though this may merely reflect the
infrequency of bites. Male Atrax robustus are generally more
dangerous than females. This may not be true for all species.
Main risks are: cardiovascular disturbance; pulmonary oedema;
acid-base disturbances; intracranial hypertension (proven in
monkeys, not in man).
Target organs: envenomation causes a complex multi-system disease
involving the cardiovascular system, lungs, central nervous
system and peripheral nervous system including the autonomic and
neuromuscular systems.2.2 Summary of clinical effectsLocal: Bite causes severe local pain, in part due to mechanical
injury from large powerful fangs. Some local erythema may
develop. Local necrosis not recorded.
Systemic: Minority of cases. Symptoms and signs may develop
within 10 minutes of the bite (if no first aid used; and more
rapidly in children than adults). The major features indicative
of systemic envenomation are:
Muscle fasciculation in the limbs involved or remote from the
bite, usually first seen in tongue or lips when systemic spread
of venom has occurred.
Marked salivation or lachrymation.
Piloerection.
Tachycardia.
Hypertension in a previously normotensive patient (late in the
syndrome the patient may become hypotensive).
Dyspnoea.
Disorientation, confusion or a depressed level of consciousness.
Note also pulmonary oedema and raised intracranial pressure.2.3 Diagnosis- Electrolytes, acid base, renal function.
- Arterial blood gases.
- Complete blood picture and platelet count.
- Serum/plasma creatine kinase.
- Urinary catecholamines.2.4 First-aid measures and management principlesThe pressure-immobilisation method is the only recommended first-
aid and has been proven effective in studies with monkeys, and in
clinical experience.
Maintain life with cardiopulmonary resuscitation measures as
indicated.
Reassure and rest the patient.
Remove spider if still attached, ensuring no further bites occur.
Immediately apply a firm broad constrictive bandage (such as
crepe) over the bite site at the same pressure as for a sprained
ankle. Extend the bandage to cover as much of the bitten limb as
possible, at the same pressure (ie, the bandage should NOT act as
a tourniquet).
Ensure immobilisation of the limb by using a splint.
Transport patient to hospital.
Do NOT give food or fluid by mouth.
Do NOT cut, suck or apply chemicals or patent medicine "cures" to
wound.
Do NOT use a tourniquet.
Treatment principles
- Maintenance of vital functions.
- Neutralisation of venom by prompt IV administration of
specific Funnel-web Spider Antivenom (CSL, Melbourne).
- General measures may include:
- Oxygen
- Atropine
- Intermittent positive pressure ventilation (also positive
end expiratory pressure, and high tidal volume may be
necessary to correct respiratory acidosis).
- Nurse patient on side due to the risk of vomiting and excess
salivation with pooling.
- Avoid fluid overload (danger of pulmonary oedema due to
envenomation); however, hypovolaemia may also develop
requiring cautious administration of albumin and volume
expanders.
- Serum sickness has not been reported following therapy with
funnel-web spider antivenom. In the event of occurrence,
steroid therapy may be worth consideration.
- Local antisepsis of wound site, and tetanus prophylaxis.
- Sympathetic blockade for hypertension and severe tachycardia
has been suggested. While alpha blockade has been used, it
requires massive doses, and beta blockade might well prove
lethal in this situation, therefore neither is advocated for
funnel-web spider envenomation.2.5 Venom apparatus, poisonous parts or organsFunnel-web spiders have paired venom production and delivery
organs, with one large fang on each end of the two chelicerae,
the fangs being paraxial, approximately 6 mm long in adult male
spiders of Atrax robustus. The venom glands are approximately 5
mm long and are connected by 4 mm long ducts to the base of the
fangs. Expulsion of venom is under at least partial voluntary
control. Detailed information on other Atrax spp. and Hadronyche
spp. not available.2.6 Main toxinsFunnel-web spider venom has only been studied in detail for Atrax
robustus, and to a lesser extent in Hadronyche formidabilis,
Hadronyche infensa, and Hadronyche versuta.
For Atrax robustus:
Yield (male spiders) - average 140 mg (dry weight).
Principal toxin - Robustoxin; protein, 4854 D, 42 amino acids.
Interferes with neuronal transmission throughout much of nervous
system. Responsible for clinical syndrome of funnel-web
envenomation, and lethality of venom.
Other components - numerous, but do not appear to have
significant role in lethal activity of venom.3. CHARACTERISTICS3.1 Description of the animal3.1.1 Special identification features
Funnel-web spiders are arthropods (phylum Arthropoda), of
the class Arachnida, order Araneae (spiders), and sub-order
Mygalomorphae (trapdoor and funnel web spiders ). They
include 35 species in 2 genera, Atrax and Hadronyche, placed
within the subfamily Atracinae, family Hexathelidae ( Gray
1988 ).
In addition to the general features of spiders, including, 4
pairs of walking limbs plus 1 pair of palps (modified as
mating organs in males) plus 1 pair of chelicerae, attached
to a rigid forebody (cephalothorax), soft, unsegmented,
petiolate abdomen and abdominal silk spinning organs (silk
glands and spinnerets), and features of Mygalomorph spiders
including 2 pairs of book-lungs visible on the ventral
abdomen, chelicerae with paraxial fangs, attached
horizontally to the cephalothorax rather than vertically;
funnel-web spiders also have the following distinguishing
characteristics (figures 3.1.1 to 3.1.11): (Gray 1987,
1988)
They are large to very large spiders, body length 15 - 45 mm
(excluding the jaws or chelicerae ), dark brown to black in
colour overall, the abdomen often dark plum coloured. The
carapace covering the front part of the body is almost
hairless and so appears smooth and glossy. The body lacks
any obvious patterning.
Spinnerets obvious, four in number, the apical segments of
the large posterior spinnerets always longer than wide
(figures 3.1.9 and 3.1.10).
Eyes closely spaced.
The labium, a small ventral plate found on the ventral
cephalothorax in the midline, immediately in front of the
sternum, and between the two maxillae, is studded with many
short peg-like spines (cuspules) (figure 3.1.11).
The fang grooves, into which the fangs fold at rest, have a
row of strong teeth along both margins (marginal teeth), and
a variable number of smaller teeth within the groove itself
(figures 3.1.7 and 3.1.8).
Carapace foveal groove concave forwards.
The tarsal segments of the legs are spined and lack thick
scopulae or claw tufts. (Figures 3.1.1 - 3.1.4.)
The second leg of male spiders may have a spur (spined
apophysis) of variable shape, on the ventral tibia (figures
3.1.1 - 3.1.3). However, males of many Hadronyche species
lack obvious apophyses (Figure 3.1.4).
Distinguishing features for each genus are:
Atrax: Carapace weakly raised and obviously longer than
wide (figure 3.1.6). Central fang groove teeth confined to
basal half of groove (figure 3.1.8). Male second leg
(figure 3.1.6) with a large, conical tibial apophysis
(figure 3.1.1). Posterior lateral spinnerets with a long
cylindrical apical segment (figure 3.1.9).
Hadronyche: Carapace moderately to strongly raised (figure
3.1.5), often almost as wide as long. Central teeth
typically occupy full length of fang groove (figure 3.1.7)
in one or several rows, but occasionally restricted to basal
region. Male second leg with a variably developed rounded
tibial apophysis (figures 3.1.2 and 3.1.3) or apophysis
absent (figures 3.1.4). Apical segment of posterior lateral
spinnerets of variable length but often rather short (figure
3.1.10).3.1.2 Habitat
They are mostly terrestrial spiders, which build typical
silk-lined tubular burrow retreats, with a collapsed
"tunnel" or open "funnel" entrance from which irregular silk
triplines radiate out over the ground. These distinctive
surface triplines, whose function is to alert the spider to
the movement of prey animals in the vicinity, provide a
reliable means of identifying the retreats of funnel web
spiders. Exceptions, which lack triplines but may have
trapdoors, are those Hadronyche from SA, viz Hadronyche
adelaidensis, Hadronyche eyrei and Hadronyche flindersi.
The silk entrance tube may be split into 2 openings, in a Y
or T form. In the case of Hadronyche formidabilis the
burrow may be in the hollow of a tree trunk or limb, many
metres above ground level.
Significant numbers of these spiders may aggregate their
burrows within a small area, forming colonies. The spiders
usually forage at the burrow entrance, seizing prey that
walks over the triplines. Adult male spiders leave the
burrow permanently to seek a mate. Such wandering male
spiders may enter houses, sometimes even find their way into
clothing, and thus account for many bites.
Most funnel-web spiders are ground or log dwellers but at
least two are tree dwellers (Hadronyche formidabilis and
Hadronyche cerberea the Northern and Southern tree funnel
web spiders respectively). They are moist-adapted animals
largely restricted to temperate to sub-tropical regions of
south east Australia in both sclerophyll and closed (rain-
forest) forest habitats. At the western edges of
distribution some species occupy dryer woodland habitats
where they dig deep burrows in sheltered microhabitats
(shaded ground in leaf litter, under rocks or logs etc).
Typically funnel web spiders prefer sheltered microhabitats
and in many urban areas these are plentiful, eg garden
rockeries, dense shrubberies, wooden sleeper or stone paths
and retaining walls and any long-term ground detritus such
as old building materials. In areas such as the damp garden
suburbs of Sydney, urbanisation may actually have increased
funnel web abundance.3.1.3 Distribution
Restricted to south-eastern Australia (figure 3.1.12).
Atrax is confined to south-eastern coastal Australia and
adjacent highlands (figure 3.1.12, 3.1.13). Atrax robustus,
the Sydney funnel-web spider, has a distribution centring on
Sydney, extending north to the Hunter River and south to the
Shoalhaven River, and narrowing westwards as far as Lithgow.
Hadronyche has a considerably wider distribution as shown in
figures 3.1.12, 3.1.14 - 3.1.18. Many species distributions
can be related to local topography (figure 3.1.19).
Overall, the distribution of Hadronyche is correlated with
the coastal trend of the eastern highlands from Tasmania to
south east Queensland, where the western trend of the main
range into dryer inland regions approximates the northern
limits of the genus (Gray 1987).3.2 Poisonous/venomous partsSee section 2.5.
Paired flask-shaped venom glands in the chelicerae connect via 4
mm venom ducts to openings at the base of the paired paraxial
fangs, approximately 6 mm long in Atrax robustus. At rest the
fangs are folded into the fang grooves on the ventral surface of
the chelicerae, but for attack the front of the body is elevated
above the prey and the fangs open downwards on widely separated
chelicerae preparatory to the downward thrust of attack. (Gray
and Sutherland 1978; Sutherland 1983)
The venom exits the fang near its tip, and is apparently under
some degree of voluntary control, as venom initially exuded on
the fang tip when the spider is threatened can then be withdrawn
back into the fang. Venom yield has been reported for Atrax
robustus as 0.28 mg for females and 0.175 mg for males, on
milking, and 0.25 mg (F) and 0.81 mg (M) on dissection of
spiders. An average figure was 140 mg dry weight. Yields are
apparently higher in summer than winter months. (Wiener 1957,
Sutherland 1983)3.3 The toxins3.3.1 Names
Robustoxin (Atraxotoxin), Versutoxin3.3.2 Description
While the venoms of most species of Hadronyche and the two
unnamed Atrax have not been studied, those known to cause
significant clinical effects in man, particularly Atrax
robustus, have been examined in detail. Consensus of these
studies is that lethal activity (for man) is contained in
just one component of these multicomponent venoms. In Atrax
robustus male venom toxicity is consistently several times
(4 - 6) higher than female venom.
Robustoxin (from male Atrax robustus venom)
(Note: A component with similar or identical properties to
robustoxin has been described by other authors, and named
atraxotoxin (and possibly atraxin). As the most complete
studies are for robustoxin, this name is adopted as the
"type" even though, historically, atraxotoxin has
precedent.) (Gregson & Spence 1981, Myelcharane et al 1983,
1984, 1985, Sutherland 1972a, 1972b, 1973b, 1983)
Robustoxin is a unique presynaptic neurotoxin, lethal in
man, other primates, and newborn mice, but non-lethal in
many other laboratory animals (or lethal only at very high
doses).
It is a protein, MW 4854 (calculated from amino acid
sequence), with 42 amino acid residues, with a high
proportion of basic residues, 8 cysteine residues with 4
disulphide bridges and has a pI &gt9 and an LD50 (SC newborn
mice) of 0.16 mg/kg. Robustoxin alone causes a typical
syndrome of envenomation in primates and man of whole male
Atrax robustus venom. (Sheumack et al 1983, 1984, 1985)
Versutoxin (from male and female Hadronyche versuta venom.)
Structurally very close to robustoxin, a protein neurotoxin,
MW 4852, 42 residues, highly basic, pI &gt9, 4 disulphide
bridges. 8 residues different to robustoxin, and considered
conservative changes. LD50 (SC newborn mice) 0.22 mg/kg.
Versutoxin alone causes almost typical syndrome of
envenomation in primates and man of whole male Atrax
robustus venom, the difference being the sustained
hypotension typical of robustoxin, which is not seen with
either versutoxin or whole Hadronyche versuta venom. Strong
antigenic cross-reaction between robustoxin and versutoxin.
(Sheumack et al, 1984)
Venoms of important related species
Hadronyche formidabilis - Venom reported as approximately
equal in toxicity (both male and female) as male Atrax
robustus venom, has caused similar cases of envenomation in
man (no definite fatalities), and therefore probably
contains a robustoxin-like component. (Sutherland 1983)
Hadronyche infensa - Venom reported as approximately equal
or greater in toxicity (females and males) as male Atrax
robustus venom, and therefore may contain a robustoxin-like
component. (Sutherland 1983)3.3.3 Other physico-chemical characteristics
Several other components or properties of male Atrax
robustus venom have been reported. These include: GABA;
Spermine Complex; Lactic acid; Trimethylsilyl or
pentafluoropropionate derivatives; Citric acid; Glycerol;
Urea; Glucose; Glycine; Spermidine; Tyramine; Octopamine.3.4 Other chemical contentsNo data4. CIRCUMSTANCES OF POISONING4.1 UsesMedical - Extraction of venom for production of antivenom and for
research.
Commercial - Some spiders killed and set in plastic for
educational purposes or, less usefully, as "tourist trophies".
Agricultural - Components of the venom may prove useful as new
insecticides, this being the subject of current research.4.2 High risk circumstancesIn areas where dangerous species occur, especially Atrax
robustus, but also Hadronyche infensa, Hadronyche formidabilis,
Hadronyche versuta, Hadronyche cerberea, Hadronyche sp.7.
- Walking barefoot, especially at night, outside places of
abode.
- Dressing in items of apparel left on or near the floor where
wandering male spiders might easily enter, including
footwear.
- Working in areas likely to have high concentrations of
spiders, eg gardens and other disturbed sheltered urban
habitats in some parts of the Sydney region.
- Activities associated with camping.
- Activities associated with handling spiders such as in
laboratories milking venom, or field researchers. NOTE: No
bites in such circumstances are recorded.
High risk times:
During the funnel web mating period male wandering activity and
abundance is highest. The summer - autumn period (December -
June) is the time of greatest activity for males of many species.
While most bites occur during this period funnel web spiders can
be encountered throughout the year. In addition pesticide
spraying to kill spiders stimulates wandering activity and
excitability in much of the target funnel web population and is
not recommended. Increased activity after heavy rainfall also
occurs because of burrow flooding.4.3 High risk geographical areasParticularly the Sydney-Newcastle-Illawarra region. See
distribution information for Atrax robustus, Hadronyche infensa,
Hadronyche formidabilis and Hadronyche versuta, section 3.1.3 and
figures 3.1.12 - 3.1.20.5. ROUTES OF ENTRY5.1 OralNot applicable.5.2 InhalationNot applicable.5.3 DermalNot recorded.5.4 EyeNot recorded.5.5 ParenteralThe only recorded route of envenomation in man is by a bite from
a spider, in most serious and all fatal cases a male Atrax
robustus. One or two fangs may enter. In most cases this is
likely to result in subcutaneous inoculation of venom.
In experimental conditions intravenous inoculation is often used,
and intramuscular and intraperitoneal injection are theoretically
applicable.
Stings do not occur (no sting apparatus).5.6 OtherNot recorded.6. KINETICS6.1 Absorption by route of exposureThe recorded method of envenomation of humans by funnel-web
spiders is purely by bite with inoculations of venom into the
skin, presumably subcutaneously in most cases.6.2 Distribution by route of exposureThe venom, when injected experimentally in monkeys, rapidly
causes systemic problems, these being immediate (IV) and delayed
about 2 minutes (SC), suggesting that the venom may be rapidly
transported from the bite site systemically. The role of
lymphatics in venom transport is uncertain, but in view of the
rapid envenomation often seen, lymphatic transport of most venom
seems unlikely. However, the compression-immobilisation
technique of first aid is effective. (Sutherland et al 1980)
Having reached the systemic circulation the main toxin (to man)
in the venom is rapidly distributed to target organs, principally
nerve cells, and particularly synaptic junctions where the toxin
is apparently bound presynaptically (autonomic and motor
neurons).6.3 Biological half-life by route of exposureThere is no published information on the half-life of the venom
or its components. Human fatalities have occurred from 15
minutes to 6 days after bites. Cases with survival following
systemic envenomation have an average hospital stay of 14 days
(if no antivenom treatment). (Sutherland 1983)6.4 MetabolismNo information.6.5 Elimination by route of exposureNo information.7. TOXINOLOGY7.1 Mode of actionStudies on the mode of action of both whole venom and Robustoxin
are hampered by low availability of venom and relative resistance
to venom in many common laboratory animals, contrasting with the
exquisite sensitivity to venom toxins in primates, including man
(50 - 100 times more sensitive in some preparations). (Sutherland
1983)
The clinical effects of funnel-web spider envenomation in man
(and monkeys) appear directly attributable to one venom
component, Robustoxin. This appears to act as a presynaptic
neurotoxin. On the autonomic system the venom causes both
inhibition of neurally mediated release of transmitters (eg
noradrenaline, acetylcholine) and an increase in spontaneous
transmitter release. A similar action on the skeletal muscle
neuromuscular junction has been postulated. (Sutherland 1983;
Sutherland & Duncan 1980, Sutherland et al 1980, Tibballs et al
1987)
Given the current paucity of relevant in vitro studies of the
mode of action of the venom, the detailed in vivo studies in
primates (Macaca fascicularis) are most relevant. In summary,
the effects recorded after experimental envenomation (IV or SC)
with whole venom from male Atrax robustus were:
Cardiovascular - initial fall in blood pressure (BP), then rise
to hypertensive level, lasting several hours, followed by return
to normal or progressive hypotension (lethal). Tachycardia,
ventricular ectopic beats, bigeminy and transient second degree
atrio-ventricular blocks were seen, though not in all monkeys.
Pulmonary oedema - seen in 3 of 9 monkeys.
Acid-base disturbances - all developed acute metabolic acidosis
about 1 hour post envenomation, resolving spontaneously by 4
hours. Most developed a respiratory acidosis.
Intracranial hypertension - seen in all monkeys.
Temperature - all developed hyperthermia.
Catecholamine excretion - marked increase in urinary
catecholamines, peaking at about 2 hours after envenomation.
Fluid shifts - all showed haemoconcentration.
Creatine kinase - all showed massive rises in CK.
Pharmacological denervation - both pre and post-envenomation
administration of atropine + phenoxybenzamine + propranolol
abolished the major features of envenomation and allowed survival
of "massive" doses of venom.7.2 Toxicity7.2.1 Human data
7.2.1.1 Adults
The lethal dose is not known, but a single bite from
an adult male A. robustus is potentially lethal and
the average venom yield is 176 mg. The recommended
initial dose of antivenom is sufficient to neutralise
in vitro about 8 times this amount of venom.7.2.1.2 Children
Children, especially those under 12 years of age, are
more susceptible to severe or lethal envenomation,
presumably due to a lower body mass and higher per kg
doses of venom.7.2.2 Animal data
Most experimental animals, being relatively resistant to the
venom, are inadequate models of human toxicity. For
experimental purposes two groups of animals appear useful,
having susceptibility to the venom of male A. robustus,
sufficient for comparative clinical studies (monkeys) or for
toxicity assay (new born mice). (Sutherland 1983, Wiener
1956, 1957)
- Monkeys (Macaca fascicularis)
lethal dose 0.2 mg/kg
- New born mice (up to 2 days old, 2 g weight)
lethal dose 1.5 mg/kg7.2.3 In vitro data
Not relevant.7.3 CarcinogenicityNo data.7.4 TeratogenicityNo data.7.5 MutagenicityNo data.7.6 InteractionsWhile not demonstrated in clinical cases, theoretically
adrenaline might have adverse effects in an envenomated patient
(and is therefore not recommended as pre-medication for antivenom
therapy), because catecholamine levels may already be elevated as
a result of envenomation. (Sutherland 1983)
Both experimentally and clinically, atropine and diazepam may
ameliorate the toxic effects of venom.
Experimentally the effects of venom (on isolated nerve-muscle
preparations) were suppressed by gallamine, suxamethonium,
lignocaine and tetrodotoxin; were enhanced by physostigmine; and
were unaffected by neostigmine, choline or acetylcholine.8. TOXICOLOGICAL/TOXINOLOGICAL AND OTHER BIOMEDICAL INVESTIGATIONS:8.1 Material sampling plan8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
Not available.8.1.1.2 Biochemical analyses
For standard tests (eg. serum/plasma electrolytes, CK,
creatinine, urea) collect venous blood in a container
with appropriate anticoagulant as issued by the
laboratory (usually heparin).8.1.1.3 Arterial blood gas analysis
Collect arterial blood by sterile arterial puncture
into a container as issued by the laboratory.8.1.1.4 Haematological analyses
For whole blood clotting time as a "bedside" test
collect 5 - 10 ml of venous blood without
anticoagulant (either in the collection syringe or
from a central line or other venous access line that
may have anticoagulant ) and place in a glass test
tube. Carefully observe the time till a clot appears.
For standard tests (eg. coagulation studies, complete
blood picture) collect venous blood in appropriate
containers with anticoagulant as issued by the
laboratory ensuring that the right amount of blood is
used (for coagulation studies citrate will usually be
the anticoagulant, while EDTA will be used for
complete blood pictures).8.1.1.5 Others (unspecified) analyses
No data.8.1.2 Storage of laboratory samples and specimens
8.1.2.2 Biomedical analyses
For samples for standard tests refer to laboratory. In
general keep at 4°C, particularly for samples for
coagulation studies.8.1.3 Transport of laboratory samples and specimens
8.1.3.2 Biomedical analyses
Use an insulated container.8.3 Biomedical investigations and their interpretation8.3.1 Biochemical analyses
8.3.1.1 Blood, plasma or serum
Electrolytes: Look for imbalance, particularly
evidence of dehydration, hyponatraemia (inappropriate
ADH syndrome?), hyperkalaemia (renal damage,
rhabdomyolysis?).
Urea, creatinine: Look for evidence of renal function
impairment.
CK: If high may indicate rhabdomyolysis (due to
secondary muscle damage), usually greater than 1000
U/l.8.3.1.2 Urine
Output: Low output may indicate renal damage or poor
fluid input.
Electrolytes if indicated (eg. inappropriate ADH
syndrome)8.3.1.3 Other biological specimens
No data.8.3.2 Arterial blood gas analyses
Performed in the setting of impaired respiratory function,
usually secondary to pulmonary oedema; look for evidence of
poor oxygenation and its sequelae.8.3.3 Haematological analyses
Whole blood clotting time: If greater than 10 mins suspect
presence of secondary coagulopathy (rare).
Coagulation studies: (if indicated clinically) If possible
these should be performed as well as or instead of whole
blood clotting time as they will give a more comprehensive
picture of any coagulopathy.8.3.5 Interpretation of biomedical investigations
The interpretation of the above tests should be made in the
context of total patient assessment including clinical
evidence of pathology such as respiratory failure, pulmonary
oedema, shock, coagulopathy and renal damage.8.4 Other biomedical (diagnostic) investigations and their
interpretation: May be indicated in response to secondary effects of
envenomation. If there is renal failure there may be a
hyperkalaemia, hence an ECG may be appropriate.
Overall interpretation of the results of the above tests will
depend on the clinical setting. Results should never be
interpreted in isolation from an overall clinical assessment.9. CLINICAL EFFECTS9.1 Acute poisoning/envenomation by:9.1.1 Ingestion
Not known.9.1.2 Inhalation
Not known.9.1.3 Skin Exposure
Not known.9.1.4 Eye contact
Not known.9.1.5 Parenteral exposure
All known cases of human envenomation are due to bites.
(Sutherland 1983)
General: In the majority of cases of funnel-web spider bite,
systemic envenomation does not occur, and any symptoms are
confined to the local effects of the bite. The outcome
cannot be predicted at the outset however, and all bites
should be assumed to be potentially lethal.
Local: One or two large fangs enter the victim with some
force. The bite is very painful for about 30 minutes or
more, with local erythema, and occasionally local
piloerection, sweating, and muscle fasciculation. Local
necrosis does not occur.
Systemic: Onset of systemic envenomation may occur from 10
minutes up to an hour or more after the bite (with further
delay if appropriate first aid used).
Earliest systemic symptoms are usually tingling around the
mouth which often occurs within 15 mins of the bite, tongue
spasms, followed by nausea and vomiting, abdominal pain,
profuse sweating, brisk salivation, lachrymation, and severe
dyspnoea.
The level of consciousness may rapidly deteriorate, with
confusion or coma. Hypertension is usually noted at this
time. Severe pulmonary oedema may develop quite early, and
is a potential cause of fatality, particularly in children.
The pulmonary oedema is mixed in origin, similar to
neurogenic pulmonary oedema, with catecholamine release,
high filling pressures, and membrane leak.
While classic neurotoxic paralysis does not occur, local and
generalised muscle fasciculation is commonly seen, including
spasms of muscle groups such as jaw musculature. In severe
cases coma has been reported, and some authors believe it
may be due to raised intracranial pressure (not relieved by
adequate control of oxygenation or BP), although this has
not been proven in man. However clinical experience
suggests coma is not common, and is probably a dubious sign
of envenomation, most envenomed patients being anxious and
alert until anaesthetized. On current experience, patients
treated with antivenom do not develop coma.
After several hours the above symptomatology may subside,
with decreased secretions, although generalised muscle
activity and coma may continue. There may be a gradual
resolution or an insidious and intractable hypotension may
develop, sometimes preceded by a brief period of semi-
normality. The hypotension may end in death due to
irreversible cardiac arrest, a possible mode of death in
fatal cases in adults, sometimes many hours after the bite.
The venom does not cause primary coagulopathy or renal
failure, though these may occur as complications.
Funnel-web spider envenomation is a complex multisystem
disease. The findings in monkeys are relevant to human
envenomation and should be consulted in conjunction with
this section (see 7.1).9.2 Chronic poisoning9.2.1 Ingestion
Not known.9.2.2 Inhalation
Not known.9.2.3 Skin contact
Not known.9.2.4 Eye contact
Not known.9.2.5 Parenteral exposure
Not known.9.2.6 Other
No data.9.3 Course, prognosis, cause of deathThe likelihood of systemic envenomation is not presently
predictable from the appearance of the bite site or local
symptoms.
The only recorded fatalities have followed bites by male Atrax
robustus. Severe envenomation not ending fatally has occurred
following bites by Hadronyche formidabilis (male specimens, but
females also considered dangerous), and H. infensa (one possible
fatal case), and more recently, H. versuta, H. cerberea, and
Hadronyche sp.7. H. versuta in any case should be considered as
potentially dangerous since its venom contains a Robustoxin-like
substance, Versutoxin. Bites from virtually all other funnel-web
spiders are unknown. A single bite from H. adelaidensis did not
result in envenomation. (Beazley 1930, Cleland 1932, Diexman et
al 1989, Fisher 1989, Fisher & Bowey 1989, Fisher et al 1980,
Fisher et al 1981, Hartman & Sutherland 1984, Ingram & Musgrave
1933, Irwin 1952, Kaire 1961, 1963, Knight & Sutton 1982, Irwin
1952, Kaire 1961, 1963, Knight & Sutton 1982, Musgrave 1927,
1949a, 1949b, Sutherland 1972c, Torda et al 1980, Watkins 1939,
White 1987, 1989, Wiener 1959).
Sutherland has noted that children usually die early in the
asphyxial stage (important role of pulmonary oedema), often
within 1 - 2 hours of the bite (shortest time 15 minutes, longest
3 days); adults die later, often due to intractable hypotension
or secondary complications, mean 11 hours (excludes one case
dying at 6 days with complications including a coagulopathy,
renal failure and brain damage). This picture is clearly
modified by the growing experience with patients treated by
specific antivenom therapy, which has proved very effective in
modifying symptomatology, and preventing a fatal outcome. 9.4 Systematic description of clinical effects(Based on both studies in monkeys and/or human cases of
envenomation prior to the development of specific antivenom).
(See refs. sect. 9.3)9.4.1 Cardiovascular
Initial fall in BP and development of tachycardia, followed
by hypertension lasting several hours, and cardiac
arrhythmias. This is followed by apparent resolution which
in severe cases indicates the onset of intractable
hypotension, and ultimately cardiac arrest in fatal cases.
Peripheral circulatory failure with peripheral cyanosis has
been recorded. (Mostly based on monkey studies.)9.4.2 Respiratory
Early development of severe pulmonary oedema (see 9.1.5.3).
While some clinicians have described this as similar to the
adult respiratory distress syndrome, with increased
pulmonary capillary membrane permeability, it appears more
similar to neurogenic pulmonary oedema, which is mixed in
origin with catecholamine release, high filling pressures,
and membrane leak.9.4.3 Neurological
9.4.3.1 CNS
Early development of impaired consciousness or coma in
severe cases has been noted, either directly due to
venom effects, or secondarily due to hypoxia
(pulmonary oedema). However, clinical experience shows
that patients do not present with or develop early
coma but are anxious and alert. Raised intracranial
pressure may develop and may be lethal (experimentally
in monkeys, not shown in man).9.4.3.2 Peripheral nervous system
Widespread effect of neurotoxic action of Robustoxin
and analogues with spontaneous transmitter release,
and failure of response to stimuli. Manifest as
muscle fasciculations, tremors, spasms, and patchy
weakness (which is usually a late manifestation).9.4.3.3 Autonomic
Widespread effect of neurotoxic action of Robustoxin
or analogues on synapses in sympathetic and
parasympathetic systems, with spontaneous release of
transmitters. Manifest as alterations in vascular
tone, and excessive secretions, especially salivation
and lachrymation, and piloerection.9.4.3.4 Skeletal and smooth muscle
Widespread effect of neurotoxic action of Robustoxin
or analogues as noted in 9.4.3.2 and 9.4.3.3.9.4.4 Gastrointestinal
Specific effects of toxin not generally noted, although
nausea and vomiting common, and gastric distension noted.9.4.5 Hepatic
No specific effects noted.9.4.6 Urinary
9.4.6.1 Renal
No specific effects.9.4.6.2 Other
Not noted.9.4.7 Endocrine and Reproductive System
Increased catecholamine excretion. Effects on pregnancy not
known.9.4.8 Dermatological
No specific effects.9.4.9 Eye, ear, nose, throat: local effects.
No specific organ injury noted, but note excessive
lachrymation, and fixed dilated pupils. 9.4.10 Haematological
No specific effects noted. Potential for secondary
coagulopathy. Fluid shifts may cause haemoconcentration.9.4.11 Immunologic
No specific effects noted.9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Acute metabolic acidosis early followed by respiratory
acidosis.9.4.12.2 Fluid and electrolyte disturbances
Fluid shift out of circulation (note pulmonary
oedema).9.4.12.3 Others
Hyperthermia is reported. Massive rises in serum
creatine phosphokinase may occur and marked
catecholamine excretion in urine (studies in monkeys).9.4.13 Allergic reactions
Not reported.9.4.14 Other clinical effects
No data.9.4.15 Special risks: pregnancy, breast-feeding, enzyme
deficiency
Pregnancy: No data. Presumed significant risk to both
foetus and mother.
Breast feeding: No data. Breast feeding unlikely to be
practically possible if severe envenomation, and in the
absence of data confirming safety, is contraindicated if
envenomation is suspected.
Enzyme deficiencies: No data.9.5 OthersNo data.10. MANAGEMENT10.1 General principlesAll cases of suspected bite by funnel-web spiders occurring in
areas inhabited by Atrax robustus, Hadronyche formidabilis, H.
infensa and H. versuta should be treated as potentially life-
threatening emergencies. This is especially true of bites to
children from male A. robustus. (See refs. sect. 9.3, also Noel
1985, Sutherland 1973a, 1978, 1983, Wiener 1978)
If appropriate first aid has not been applied and it is within 2
hours of the bite, or symptoms of systemic envenomation are
present, then it should be applied prior to assessment at a
funnel-web spider treatment centre. If first aid has been
applied it should be left in place until the patient is at a
treatment centre (exception: arterial tourniquet where viability
of limb is at stake, but beware rapid massive envenomation on
removal). For relevant first aid see section 2.4.
Main principles of medical management are:
(a) Maintain life through general measures including life
support systems if indicated.
(b) Neutralise venom with specific antivenom (Funnel-web spider
antivenom, CSL, Melbourne) if systemic envenomation is
present.
(c) Strive to avoid secondary complications, eg hypoxia and
hypoxic damage, brain damage, renal failure, coagulopathy.10.2 Relevant laboratory analyses and other investigations10.2.1 Sample collection
Blood and urine for biomedical analysis.
Request if possible the capture of the spider for
confirmation of species and sex. Dead spiders may be
preserved in either ethanol, or methanol, preferably 70%
strength.10.2.2 Biomedical analysis
There are no specific assays for funnel-web spider venoms.
All tests are to determine the extent of effects of venom
systemically, e.g.
(a) Arterial blood gases - extent of hypoxia and response
to treatment.
(b) Serum/plasma electrolytes, acid base, renal function -
extent of metabolic acidosis, secondary renal
impairment.
(c) Serum creatine kinase - secondary elevation.
(d) Complete blood picture - early evidence of secondary
coagulopathy, haemoconcentration.
(e) Coagulation studies - required if suspicion of
secondary coagulopathy (rarely present, not usually
seen acutely in the first 8 hours after bite).
(f) Urinary catecholamines - may be significantly
elevated.10.2.3 Toxicological analysis
No specific venom analysis available. See Section 8.10.2.4 Other investigations
Not applicable.10.3 Life supportive procedures and symptomatic treatmentSevere funnel-web spider envenomation is a complex multi-system
disease. This is best managed in an ICU setting, preferably in a
treatment centre with previous experience in handling such cases.
(a) IV line - urgently establish good IV line access.
(b) Respiratory - severe pulmonary oedema causing hypoxia and
respiratory failure demands urgent ICU management which
classically includes intubation and mechanical ventilation
(intermittent positive pressure ventilation (IPPV); positive
end expiratory pressure (PEEP), oxygen, possibly high dose
steroids (now believed to be contraindicated), and later,
and possibly diuretics (value uncertain). CVP line,
arterial line, and Swan-Ganz catheter have proved valuable
for monitoring. (Note: see section 11.1 for detailed
review of management of pulmonary oedema in these cases.)
(c) Circulatory - managed in conjunction with respiratory
problems. May require isoprenaline, and volume replacement
with SPPS or albumin. Dopamine infusion, suggested by one
author, is probably contraindicated.
In the early stages where hypertension and tachycardia are a
problem, sympathetic blockade has been suggested. While
alpha blockade has been used, it requires massive doses, and
beta blockade might well prove lethal in this situation,
therefore the writers do not advocate the use of either for
funnel-web envenomation.
(d) Pharmacologic - atropine has proved valuable, eg for
parasympathetic blockade. Diazepam has also been suggested,
but only when ventilation is supported.10.4 DecontaminationNo data. Local suction unlikely to be useful. There is some
suggestion that prolonged immobilisation of venom at the bite
site using recommended first aid (see Section 2.4) may allow
local destruction of venom.10.5 EliminationNo data.10.6 AntidoteThe availability since 1981 of specific funnel-web spider
antivenom (CSL, Melbourne) has dramatically changed the pattern
of funnel-web spider bite envenomation sequelae. In all cases
where envenomation has occurred antivenom is the definitive and
preferred treatment. (DIEKMAN et al 1989, Fisher et al 1981,
Hartman & Sutherland 1984, Sutherland 1980, 1983, Sutherland et
al 1981)
Sutherland has defined the following as clinical indicators of
systemic envenomation by male A. robustus. The presence of any
of the following is an indication for antivenom:
(a) Muscle fasciculation in the limb involved or remote from the
bite, usually first seen in tongue or lips when systemic
spread of venom has occurred.
(b) Marked salivation or lachrymation.
(c) Piloerection.
(d) Significant tachycardia.
(e) Hypertension in a previously normotensive patient.
(f) Dyspnoea.
(g) Disorientation, confusion, or a depressed level of
consciousness.
In most cases of bites by funnel-web spiders, no symptoms will
develop other than local pain of limited duration due to the
mechanical trauma of the bite. These patients do not require
antivenom.
Funnel-web spider antivenom is prepared by hyperimmunising
rabbits with male A. robustus venom, and is therefore a rabbit
immunoglobulin. The average quantity per ampoule is 100 mg of
purified rabbit IgG, which is enough to neutralise in vitro the
average venom yield from at least 4 adult male A. robustus.
Sutherland recommends prophylactic pretreatment with
antihistamine and a steroid, about 15 minutes prior to antivenom.
Pre-medication with adrenaline is not recommended. Subcutaneous
testing for allergy is not recommended. The antivenom should be
given intravenously, initially very slowly. The initial dose is
a minimum of 2 ampoules, or 4 ampoules for a severe case, and
repeated in 15 minutes if no improvement. As with all
antivenoms, everything should be prepared to treat anaphylaxis
should it occur; however, anaphylaxis has not been reported in
these cases and theoretically it is unlikely it could occur in
severe cases due to the neuroendocrine response. The dosage is
the same for children and adults. Serum sickness has not occurred
following therapy with funnel-web spider antivenom. In the
unlikely event of occurrence, steroid therapy may be worth
consideration.10.6.1 Adults
Minimum 2 ampoules, most cases will require 4 or more
ampoules.10.6.2 Children
As for adults.10.7 Management discussion: alternatives, controversies, research
needs See also section 11.1
While systemic envenomation by male A. robustus and some other
funnel-web spiders is a severe, potentially fatal complex multi-
system illness, the advent of specific antivenom has
significantly modified the likely outcome and problems
encountered. Its development and dissemination by Sutherland and
colleagues at CSL Melbourne has been the crucial step in
ameliorating this envenomation syndrome and dramatically reducing
the likelihood of fatalities. As a result, much of the pre-
antivenom controversy about management practices and medication
is now largely redundant. The important work of Fisher and
others had established valuable precedents in the successful
treatment of severe envenomation in an ICU setting, prior to
antivenom becoming available (see section 11.1 and Fisher et al
1980 for a detailed discussion). Similarly, Sutherland's work on
first aid methods, initially controversial, is now widely
accepted as the standard, with little active dissent, although
tourniquets are still wrongly used as first aid in a disturbingly
high number of cases. Of more importance is the finding that in
many cases no first aid has been used, a situation which is most
disturbing considering the rapidity of onset of life threatening
problems in severe cases and the effectiveness of correct first
aid in delaying such problems. Possibly even more vigorous
public education would help.
While the development of a venom assay, akin to those developed
for Australian snake venoms, might allow further clinical and
experimental study of venom actions, because of the nature of
funnel-web spider envenomation compared to snakebite, it would
not be likely to have the same clinical impact as the snake Venom
Detection Kit (CSL Melbourne), and from both a clinical
management and economic viewpoint is of quite dubious value. The
antivenom prepared against A. robustus venom has now been shown
potent against bites by other species.11. ILLUSTRATIVE CASES11.1 Case reports from the literatureFisher et al, 1980
Very detailed report of 2 severe, non-fatal cases, which
constitute an excellent guide to successful management if
antivenom unavailable. Both cases are therefore given in some
detail.
Case 1
RB, a 23 year old previously healthy man, was bitten twice on the
left knee by a male funnel-web spider (Atrax robustus) while
rock-climbing. An arterial tourniquet was applied above the site
of the bite immediately. The spider was killed and kept for
identification purposes and the patient assisted to Royal North
Shore Hospital by his companions.
On arrival, some 30 minutes after the bite, he complained of
burning pain on the inside of his left thigh, extending to his
groin. He noticed circumoral paraesthesia, spasms of his tongue
and palate, followed by agitation, sweating, lacrimation,
salivation and blurred vision. He vomited twice and complained
of increasing dyspnoea. His blood pressure was 160/100 mmHg,
heart rate 120/minute, and his left pupil was fixed and dilated.
He had spasm and rigidity of proximal and distal muscles in both
upper and lower limbs.
He was given atropine 0.6 mg and diazepam 5 mg intravenously and
a further 5 mg diazepam and transferred to the Intensive Therapy
Unit. Chest X-ray showed diffuse interstitial pulmonary oedema
and a normal cardiac shadow: blood gases breathing room air were
PaO2 56 mmHg, PaCO2 22 mmHg, pH 7.37. His haemoglobin (Hb) was
17.2 g/100 ml.
The tourniquet was released and oxygen administered with a Hudson
non-rebreathing mask with a flow of 12 litres/minute. He
deteriorated rapidly developing increasing dyspnoea, gross
peripheral vascular shutdown and cyanosis while his blood
pressure rose to 210/120 mmHg. There was no response to further
increments totalling 45 mg of diazepam intravenously and his
ventilation was assisted with a Mapleson D breathing circuit with
100% oxygen. He was given suxamethonium 100 mg. As muscle
relaxation occurred vast quantities of pink frothy oedema fluid
poured from his mouth and onto the floor, making endotracheal
intubation extremely difficult. He was paralysed with
pancuronium and commenced on intermittent positive pressure
ventilation (IPPV) with 100% oxygen and a tidal volume (TV) of
one litre and a rate of 14 breaths/minute. Peak pressure was 45
cm H2O and plateau pressure 35 cm H2O (Elema Schonander 900B
ventilator).
Following the institution of ventilation a positive end-
expiratory pressure (PEEP) was applied and rapidly increased
until the oedema fluid was absent from the tubing. The PEEP
level necessary was 20 cm H2O. He was given methylprednisolone 2
g and frusemide 40 mg. There was no diuresis. His right pupil
became fixed and dilated. A central venous catheter was inserted
and his central venous pressure (CVP) off the respirator was 25
cm H2O (zero reference point mid axillary line). On each
occasion that the patient was disconnected from the ventilator or
the PEEP reduced, copious pink frothy fluid poured into the
respirator tubing.
Analysis of the pulmonary oedema fluid taken four hours after
admission showed high levels of protein. When ventilation (FiO2
= 1) was stabilised blood showed PaO2 346 mmHg, PaCO2 68 mmHg, pH
7.1. The minute volume was increased to 22 litres over a period
to bring PaCO2 to normal levels and correct the acidosis.
After 90 minutes his blood pressure began to fall and PaO2 on
100% oxygen fell to 117 mmHg. He was treated with infusion of
25% albumin 500 ml over one hour which reduced the Hb
concentration to 16.2 g/100 ml. Over the next four hours he was
given 500 ml of stable plasma protein solution 5% (SPPS) and a
further 200 ml of 25% albumin. The vasoconstriction was not
improved by chlorpromazine 25 mg intravenously and an
isoprenaline infusion was commenced at the same time as the
albumin infusion. His pulse slowed and peripheral perfusion
improved over about 30 minutes.
Eight hours after intubation his spontaneous tidal volume was
1200 ml and he was fighting the ventilator. He was extubated and
commenced on salt and water restriction and intermittent
frusemide to produce a negative salt and water balance. His
radiological appearance and alveolar-arterial gradient
deteriorated markedly on extubation but over the next few days
progressively returned to normal. He had episodes of high fever
over the next five days. His complement levels and clotting
screen were normal, CPK and fibrin degradation products were
minimally raised. He was discharged well 13 days after admission.
Case 2
RT, a fit 40 year old woman, was bitten on the distal phalanx of
her left index finger by a spider positively identified as a male
Atrax robustus. The spider had to be prised from her finger and
the wound bled profusely. An arterial tourniquet was applied and
she was taken to Woy Woy District Hospital. The tourniquet was
released with no untoward effects and she was transferred to
Gosford Hospital.
On arrival 40 minutes after the bite she complained of perioral
tingling, anxiety and nausea. Her pulse rate on admission was
120 and over the next 30 minutes fell to 34 beats/minute with
blood pressure 190/110 mmHg. ECG at this time showed blocked
atrial escape which reverted to bi-directional tachycardia after
atropine 0.6 mg intravenously.
Over the next two hours she became progressively more
hypertensive and flushed, her left pupil became fixed and dilated
and eyes became puffy. She developed marked peripheral
vasoconstriction. She was given diazepam 10 mg intravenously
with no noticeable effect and transferred to the Intensive Care
Unit. Her chest was clear. Three and a half hours after the
bite she was dyspnoeic with generalised crepitations over all
lung fields; blood pressure was now 170/110 mmHg, pulse rate 130.
Chest X-ray showed bilateral interstitial and alveolar oedema and
blood gases on room air were PaO2 46 mmHg, PaCO2 28 mmHg, pH 7.3.
She became progressively more breathless and, four hours post-
bite, minor muscle spasms developed along with peripheral
cyanosis and gross vasoconstriction. She was given diazepam 20
mg, atropine 0.6 mg and suxamethonium 100 mg and an endotracheal
tube was inserted with difficulty, due to profuse pulmonary
oedema which poured on to the bed and floor. She was commenced
on IPPV and controlled with pancuronium and diazepam. PEEP was
applied until airway flooding ceased at 10 cm.
Her haemoglobin was 16.2 g/100 ml. CVP reading was 16 cm H2O.
She rapidly developed hypotension which was treated with albumin
infusion and isoprenaline infusion. As her blood pressure
improved her peripheral vasoconstriction decreased. She was
given 2 g hydrocortisone; the albumin infusion was continued for
episodes of hypotension. Over 24 hours she received two litres
of 25% albumin which brought her haemoglobin down to 10 g/100 ml
and was associated with continuing improvement in arterial blood
gases. In the second 24 hours she received a further 600 ml of
albumin and an increase in PEEP to 20 cm was required to maintain
oxygenation.
Over the next 24 hours she became oliguric. She was given 500 ml
of Ringer's lactate, immediately developing profuse airway
flooding in spite of high levels of PEEP. This ceased within
minutes of stopping the infusion. She was given two doses of
frusemide 80 mg with little response. Forty-eight hours after
admission to Gosford she was transferred to Royal North Shore
Hospital.
On arrival she was stabilised on a Servo volume-cycled ventilator
delivering 80% oxygen with 20 cm of PEEP and minute volume 10
litres. Arterial blood gases were PO2 110 mmHg, PCO2 50 mmHg, pH
7.42. A Swan-Ganz catheter was inserted and pressures recorded
were pulmonary artery (PA) 40/26 mmHg, and mean pulmonary
capillary wedge pressure (PCWP) 23 mmHg, CVP 26 cm H2O.
Reduction of PEEP led to immediate airway frothing. She was
given frusemide 250 mg and methylprednisolone 2 g six-hourly for
24 hours. 1000 ml of blood was removed by phlebotomy over two
hours bringing mean PCWP to 17 mmHg. A diuresis began and she
passed in excess of 40 ml urine hourly over the next 16 hours.
She was given 500 ml of packed cells over four hours to restore
the haematocrit. Twenty-four hours after arrival she was on 20
cm of PEEP, PCWP (mean) was 13 mmHg, and blood gases on FiO2 0.45
were PaO2 101 mmHg, PaCO2 37 mmHg, pH 7.47. Six hours after
admission she developed a high fever which persisted 48 hours.
Blood cultures were negative.
She became oliguric and unresponsive to increasing dosage of
frusemide. Serum creatinine was 0.31 mmol/l. She was given 500
ml of fresh frozen plasma and mean PCWP increased to 17 mmHg and
was associated with a brisk diuresis. She was continued on salt
and water restriction and artificial ventilation. On the 4th day
reduction of PEEP was not followed by airway frothing and she was
commenced on intermittent mandatory ventilation. The
isoprenaline was ceased.
On day 5 she was extubated with radiological deterioration of
lung function after extubation. On day 6 her serum creatinine
was normal, she was commenced on a light diet and fluid intake
was gradually increased. She was extremely weak for five days
and was gradually mobilised over the next week and discharged
well 20 days after the bite.
Clotting screen and complement levels were normal throughout the
illness, CPK and liver function tests were marginally raised.
Discussion (From original paper, edited).
Pulmonary oedema due to the bite of the male funnel-web spider
has been well documented and may be a feature of seriously ill
envenomated patients.
In the period 1940 to 1978, 33 patients were admitted to Royal
North Shore Hospital with a history of spider bite. Only three
had major symptoms and these were all envenomated by male funnel-
web spiders. Symptoms were predominantly pulmonary oedema and
cardiovascular. One patient recovered spontaneously and two
died.
The clinical features in the two patients with definite male
Atrax robustus envenomation were:
(1) Pulmonary oedema
Pulmonary oedema is produced when fluid enters the pulmonary
interstitium at a rate exceeding pulmonary lymphatic drainage.
Clinical features appear when the interstitial volume is six
times normal. The oedema may occur due to disturbance of any of
the factors governing fluid movement in the lung. One of these
with possible relevance to funnel web spider envenomation is
increased pulmonary capillary membrane permeability (PCMP), which
is an increasingly recognised form and usually the most severe,
although only moderate changes in permeability are required and
they may be short-lived. Under some circumstances increased PCMP
may not produce oedema without raised capillary pressure. Both
cases described showed a protein content suggestive of increased
PCMP oedema. The initial washout of interstitial protein may be
beneficial in increasing plasma-tissue osmotic pressure gradient,
but the loss from plasma to interstitium promotes greater
movement of fluid into the interstitium and leads to reduced
clearing and eventual organisation and fibrosis in the alveoli.
In hydrostatic pulmonary oedema, PEEP does not retard lung water
accumulation although in increased PCMP oedema due to sepsis it
protects against the effects of volume loading. There is no
benefit in raising COP in increased PCMP pulmonary oedema.
Because of the evidence of massive sympathetic discharge, severe
vasoconstriction, high protein oedema and the lack of
experimental evidence of an effect of the venom on the pulmonary
capillary membrane in animals, it is possible that the mechanism
of the pulmonary oedema due to Atrax robustus venom may either be
"neurogenic pulmonary oedema" or a direct effect of toxin or
mediator on the pulmonary capillary membrane.
Our approach to the therapy of the pulmonary oedema in both
patients was to control ventilation with increasing levels of
PEEP until airway flooding ceased, to restore blood volume with
colloid solutions, and to carefully dehydrate the patients when
volume was restored and airway flooding ceased, which avoided the
dangers of diuretic therapy in the presence of hypovolaemia. The
combination of albumin to raise COP and maintain blood volume
with diuretics to reduce extracellular fluid volume has been used
successfully to treat pulmonary oedema by a number of authors.
Although PEEP may not alter fluid dynamics in the lung and
usually improves oxygenation by opening closed alveoli, the PEEP
in these circumstances stopped large airway flooding and allowed
volume restoration and maintenance of COP. PEEP may often
produce marked improvement in chest radiography due to opening of
alveoli and increased functional residual capacity. The dramatic
deterioration in X-ray after institution of spontaneous
ventilation and cessation of PEEP in Case 1 we felt was of such
magnitude as to represent a true deterioration in oedema over and
above the cosmetic effects of PEEP. The high levels of PEEP
required to stop large airway flooding led to over-distension of
the lung, and the difficulty in removal of CO2 could have been
related to increased dead space as a consequence of excessive
PEEP or increased CO2 production.
The use of Ringer's lactate solution in Case 2 was associated
with prompt appearance of airway frothing which was not
controlled by increasing PEEP. Suction was avoided in these
patients until airway frothing had ceased to avoid applying
negative pressure to the alveoli. Removing the PEEP to measure
central venous pressure was associated with massive airway
flooding and is at best a hazardous and probably unnecessary
practice. Both patients required a high minute volume initially
to achieve normocarbia.
In addition we used high dosage steroids in both patients, in
Case 1 once only and in Case 2 for 72 hours. Sutherland states
that there is no evidence that steroids affect the clinical
course in Atrax envenomation, and while acknowledging that these
patients do not provide such evidence, we believe they should be
given for their potential benefit, in producing fall in total
peripheral resistance, improvement in oxygenation and pulmonary
oedema, stabilisation of pulmonary capillary membrane, shift in
haemoglobin dissociation curve to the right and decreased
pulmonary vascular resistance.
(2) Circulatory changes
The venom causes vasoconstriction, potentiation of response to
noradrenaline, and a biphasic response in rabbit atria with
initial depression followed by stimulation related to
noradrenaline release. Both patients showed hypertension and
tachycardia on admission. Case 2 developed a bizarre arrhythmia
shortly after admission which responded to atropine. Case 1 had
supraventricular tachycardia for the first four hours.
The most marked feature was the gross peripheral vasoconstriction
which was associated with hypertension and tachycardia. This was
associated with right and left cardiac failure and
haemoconcentration. The haemoconcentration occurs due to plasma
loss, and in the absence of blood loss has been used to
quantitate plasma loss.
Isoprenaline appeared effective in reducing vasoconstriction and
lowering blood pressure in these patients and was initially
associated with a slowing of the pulse rate.
Hypovolaemia may have contributed to the subsequent development
of hypotension in these patients, and in Case 1 treatment of
failure and vasoconstriction with isoprenaline and blood volume
restoration with albumin and SPPS to normalise haematocrit
promptly restored circulation. In Case 2 oxygenation improved
while two litres of 25% albumin was given, but further increments
produced a deterioration in lung function which was corrected by
venesection and diuresis.
Restoration of blood volume in the presence of increased
pulmonary capillary membrane permeability (PCMP) is a
controversial subject. Colloid solutions have been used to
replace volume and raise colloid osmotic pressure and it has been
suggested that albumin and dextran may act to "plug the leak".
However, these solutions may leak into the pulmonary interstitium
making the situation worse. They have the advantage of restoring
volume while avoiding salt and water excess with over-expansion
of interstitial water.
In Case 1 the use of high level PEEP and albumin in combination
enabled restoration of normal haematocrit with continuing
improvement of alveolar-arterial gradient which is evidence
against loss of albumin into the interstitium. Case 2 improved
in a similar fashion until overloaded, and was improved
dramatically by venesection and lowering of PCWP.
(3) Pupillary changes
Both patients showed unilateral fixed dilated pupils on the side
of the bite proceeding to bilateral fixed dilated pupils for a
four to six hour period. At no time was there evidence of
papilloedema.
(4) Muscle spasms
These occurred as an early manifestation in Case 1 and a late
manifestation in Case 2. The recommended treatment for such
spasms is diazepam intravenously. Diazepam did not appear
effective in Case 1 and its efficacy could not be assessed in
Case 2 as a small dosage was given prior to muscle spasms. The
administration of repeated dosages of diazepam to patients who
have pulmonary symptoms after Atrax envenomation we would regard
as contraindicated in the absence of demonstrated efficacy in
humans, because of the hazards of repeated administration of
respiratory depressant drugs in respiratory failure. The use of
ventilatory support and non-depolarising relaxants would seem a
safer way of blocking the effects of acetylcholine while
improving the ventilatory status.
(5) Renal function
Both patients developed elevation of serum creatinine. Urinary
electrolytes were unhelpful in assessing the patients in the
early stages due to the use of frusemide. In Case 2 concentrating
ability and sodium retention were normal on day 4 in spite of a
serum creatinine that rose to 0.33 mmol/l.
Case 1 was found to have hyaline casts in his urine and Case 2
had no abnormal sediment. There is no experimental evidence of a
nephrotoxic effect of the venom and the renal impairment may well
have been related to the circulatory disturbance consequent on
the profound vasoconstriction and the well documented effects of
high levels of PEEP, or reduced glomerular filtration due to
elevated serum protein levels.
It was interesting to note that oliguria persisted in Case 2
after 500 mg frusemide when there was a mean pulmonary capillary
wedge pressure (PCWP) of 13 cm H2O but following subsequent
elevation of the PCWP to 16 cm H2O with plasma there was an
immediate diuretic response, without changes in blood pressure,
pulse rate or CVP.
Hyperglycaemia occurred in both patients in the early phase.
This may have been due to sympathetic activity or steroids.
Perioral tingling was the first symptom in both patients.
Excessive salivation occurred in both patients. Atropine in the
dosages given (0.6 mg) did not reduce this and higher dosages
should be used. Intermittent pyrexia occurred in both patients,
as a late manifestation.
Management of envenomation due to Atrax robustus.
The deterioration in Case 1 after tourniquet release was dramatic
and we endorse the view of Sutherland and Duncan that a pressure
immobilisation bandage should be applied. An arterial tourniquet
is also effective but hazardous and painful. Whatever means are
used to delay systemic effects, they should not be released until
the patient is in hospital. We would endorse the use of
atropine, in higher dosage than we used, for control of
secretions and bradycardia.
For reasons outlined earlier we find it difficult to support
Sutherland's advocacy of diazepam if there are respiratory
symptoms. We believe that pulmonary oedema and circulatory
failure due to envenomation by Atrax robustus should be treated
by:
1. artificial ventilation and levels of PEEP sufficient to
prevent airway flooding;
2. high dose steroids;
3. blood volume replacement with albumin;
4. circulatory support and treatment of vasoconstriction with
isoprenaline, phentolamine or nitroprusside;
5. fluid restriction and diuretic therapy when the airway
flooding phase has ended;
6. during fluid replacement Hb and CVP should be measured and
in severe cases Swan-Ganz catheterisation is indicated.
However, rather than rigid adherence to protocols of management
it is essential for successful outcome in the management of these
patients that careful application of modern principles of
assessment, therapy and repeated measurements be used in
treatment.
Musgrave, 1927
Case 1
Child (? age 2 years), outcome fatal. Presumed A. robustus.
The boy was bitten on the 5th digit, left hand, at home in
Thornleigh (Sydney); he immediately commenced crying. Tourniquet
applied. When seen medically the child was unconscious, deeply
cyanosed, and in a state of chronic convulsive spasm. Treatment
not detailed. Died 1.25 hours after arrival and "a few hours"
after the bite (Sutherland, 1983, lists death as occurring 1.5
hours after the bite). This case is apparently the first recorded
fatality from funnel-web spider bite in Australia.
Case 2
Adult man, 42 years, non-fatal. "Male A. robustus".
Trod on spider, causing bite to foot, with 2 punctures, and local
pain "similar to that of a bee-sting"; 35 minutes later developed
numbness of tongue, loss of taste, and "twinging pain in the
tongue and lips". By 1.5 hours, pain had extended to both hands
and feet and, by 2 hours, he developed excessive salivation,
nasal discharge, twitching of facial muscles, especially lips,
and facial parasthesiae. By 3 hours developed lachrymation,
could only control eyelids with difficulty, had nausea, a choking
feeling in the throat. At about 3.5 hours, blurred vision,
difficulty controlling limbs, and peripheral coldness and
numbness occurred. All symptoms became progressively worse over
the next 2 hours. Symptoms continued over the next 12 hours or
so, but with some relief by the next day, over 24 hours post-
bite. Steady improvement over the next 2 days.
Case 3
Adult man, non-fatal. Male H. formidabilis.
Bite to the buttock while dressing one night (spider in
trousers), then bite to finger. Intense local pain initially,
then numbness. By 3 hours had developed "intense vomiting,
profuse perspiration, violent cramps in the limbs and abdominal
muscles", delirium, bradycardia (60 bpm), laboured respirations
and "coughing up quantities of mucous, saliva trickling from the
mouth, and pupils contracted". No further details though the
patient survived (further details in Ingram and Musgrave, 1933).
Beazley, 1930
46 year old woman, outcome fatal. Male A. robustus.
Bitten on left thumb; 40 minutes later had a red congested face
with cold clammy periphery, thready pulse, and hypotension
(systolic BP 55 mm Hg). She then developed "incessant retching
of thick tenacious mucus", then an hour later, dyspnoea,
pulmonary oedema, laryngeal spasms, facial cyanosis, and apparent
peripheral shutdown. Atropine had no clinical effect. About 4
hours post-bite she had moderate cyanosis, frothing at lips,
clonic contractions of arms and legs every 10-20 minutes,
bilateral small fixed pupils, and a tachycardia. The bite site
had 2 minute punctures, without local oedema. By 6 hours post-
bite she was comatose. She died at 9 hours post-bite.
Autopsy showed oedematous lungs with fine froth throughout the
airways, and alveolar distension. Some congestion was seen in
the liver, kidneys and stomach wall. No cerebral lesions were
seen.
Ingram and Musgrave, 1933
Case 1
Young adult woman (? age 25 years), outcome fatal. Presumed A.
robustus. Bitten on buttock while sitting on grass, causing sharp
local pain. Within 10 minutes was "pale, felt weak and ill, and
commenced to perspire freely". She subsequently collapsed, with
"marked dyspnoea and inspiratory stridor". No local reaction at
the bite site. She produced frothy fluid from the airways, and
vomited frequently. A hyperthermia (38°C) was noted with
tachycardia (150 bpm) and tachypnoea (50 bpm). "Analgesia of the
whole body was observed" and the pupils were small and
unreactive. Tendon reflexes sluggish. She developed progressive
cyanosis and "died suddenly from heart failure 13 hours after
being bitten". Autopsy revealed acute pulmonary oedema.
Case 2
Boy, 7 years, outcome non-fatal. Male A. robustus. Bitten on
right hand, causing local pain; 30 minutes later had severe
dyspnoea with frothing at the mouth, and shortly thereafter had
"signs of acute lung oedema", tachycardia (130 bpm), marked
inspiratory stridor, constant vomiting, paralysis of
accommodation, unable to open mouth, and apparent right facial
weakness. Morphine and atropine appeared to give temporary
relief, but he again developed vomiting, dyspnoea, tachycardia,
and abdominal rigidity, priapism, and arreflexia. A lateral
nystagmus was noted, and generalised muscle tenderness. Cyanosis
developed, then coma, and a venesection (200 ml) was performed.
This gave rapid relief and within 30 minutes he was able to
drink, and he continued to complete recovery.
Wiener, 1961
Lists 10 fatal cases (including those in 11.1.2 and 11.1.3) since
1927.
Torda et al, 1980
A detailed case report.
Female, 31 years, outcome fatal. Male A. robustus. Bitten on
wrist. Use tourniquet first aid. At 30 mins noted blurred
vision and sweating, and at 60 mins, muscular twitching and then
generalised spasms, followed by profuse salivation, nausea and
vomiting, and respiratory difficulty (PaO2 46 mmHg while on
oxygen at 6 L/min). By 3 hours post-bite she was stuporous,
cyanosed, irritable, tachypnoeic, tachycardic (180 bpm) with
frequent ventricular ectopics, hypertensive (160/110), and had
generalised muscular spasms. She had severe pulmonary oedema and
at about 3 hours post-bite was paralysed, intubated and
ventilated with IPPV and PEEP on 100% O2, giving a PaO2 of 91
mm/Hg.
She remained stable for 4 hours, then at about 6-7 hours post-
bite she became severely hypotensive and anuric, with sluggishly
reactive dilated pupils. She was resuscitated with 1.5 L SPPS,
dopamine infusion (10 mg/kg/min), and digoxin 0.5 mg IV, with
return of urine output, contraction of pupils, and rise in BP (to
80-100 mmHg) by 11 hours post-bite. By next day (24 hours post-
bite) she was awake but falling PaO2 required increased PEEP.
She was assessed as having continued pulmonary oedema consistent
with adult respiratory distress syndrome. Further falls in PaO2
were initially managed with increased PEEP with secondary
pneumomediastinum.
By day 3 she developed severe peripheral cyanosis and an apparent
DIC-type coagulopathy, and raised liver enzymes and creatinine.
Deterioration continued, and by day 4 she was unconscious, and
she required PEEP and continuous dopamine infusion, peripheral
cyanosis worsened, and heparinisation instituted for the
coagulopathy.
On the 5th day there was deterioration in cerebral function, with
poor response to painful stimuli, papilloedema, and EEG
deterioration, and hyperthermia. By the 6th day she was anuric,
developed further unresponsive hypotension, and died in asystole.
Fisher et al, 1981
Report of first 2 cases treated (successfully) with specific
funnel-web spider antivenom.
Case 1
Male, 49 years, bitten on foot by a male A. robustus.
Compression bandage first aid applied. 15 mins post-bite he had
local pain, sweating, piloerection, and perioral tingling,
shortly followed by muscle fasciculation of the arms progressing
to severe spasm, then nausea, vomiting, marked salivation and
lachrymation. By 25 mins there was evidence of pulmonary oedema
and hypertension (240/140). By 50 mins there was stridor and
cyanosis, and he was intubated. He was then transferred to
another hospital, by which time (75 mins post-bite) there was no
evidence of pulmonary oedema, but continued hypertension, a
metabolic acidosis, tachycardia, and increased muscle tone.
Following pretreatment with promethazine and methylprednisolone
he received 7.5 ml funnel-web antivenom IV, and 15 mins later a
second dose. Over the next hour his BP reduced to normal, HR
reduced to 120 bpm, and muscle tone reduced. The improvement
continued and he was discharged less than 2 days post-bite. His
only residual problem was excessive sweating for 3 weeks.
This case illustrates a marked beneficial response to antivenom
in severe envenomation, with significant reduction in length of
hospitalisation and complications.
Case 2
Male, 3 years, bitten on the toe by a male A. robustus.
Tourniquet applied as first aid. Within minutes of removal of
first aid, developed acute distress, marked salivation,
lachrymation, sweating, piloerection, hypertension, tachycardia,
then pulmonary oedema, cyanosis, and disorientation. He was
intubated and ventilated with PEEP, but with continued pulmonary
oedema. Funnel-web spider antivenom was then administered IV
following premedication with promethazine and methylprednisolone.
Over the next hour there was a steady improvement, and extubation
was possible 75 mins later. He was discharged the following day,
and had no further problems.
This case again illustrates severe envenomation rapidly resolved
by antivenom therapy, with consequent reduction in
hospitalisation.
Knight and Sutton, 1982
Male, aged 9 years, bitten on a finger by a male Hadronyche
formidabilis. By 10 mins he was vomiting, sweating, with local
pain, and by 15 mins he was pale, sweaty, tachycardic (160 bpm)
and hypertensive (140/110). He was transferred by air to Sydney,
and on arrival, 2 hours post-bite, he had fasciculation of
tongue, poor peripheral perfusion, with a tachycardia (150 bpm),
and hypotension (85 systolic), but no evidence of pulmonary
oedema. After pre-treatment with promethazine and
hydrocortisone, he received funnel-web spider antivenom IV (2
ampoules), with rapid improvement thereafter. However symptoms
returned, necessitating a further 2 ampoules of antivenom about
one hour later. Again there was rapid improvement but a further
relapse 2 hours later, which stabilised spontaneously without
more antivenom therapy, and 3 hours later he was substantially
well, being discharged 3 days post-bite.
Hartman and Sutherland, 1984
This paper documents 9 cases of funnel-web spider envenomation
treated successfully with specific antivenom. All had severe
envenomation, and showed clear improvement following antivenom
therapy. The duration of hospitalisation was 1-3 days, compared
to 2-3 weeks prior to antivenom availability.
Each case is briefly discussed. The first three cases are those
presented in 11.1.7 and 11.1.8 above. In discussion it is
suggested that correct first aid may reduce the incidence of
severe envenomation by allowing some local inactivation of the
venom.
Fisher and Bowey, 1989
Review of cases of envenomation admitted to one ICU over 12
years. 35 patients admitted with funnel-web spider bite. 8 of
these had severe envenomation, 6 requiring artificial
ventilation, and all showed pulmonary oedema, hypertension,
tachycardia, and muscular spasms. Average duration of
hospitalisation in these 8 cases: 9.6 days (no antivenom), and 2
days (antivenom therapy). Diekmann et al 1989.
Diekmann et al 1989
Description of 3 cases of significant envenomation by Hadronyche
versuta, H. infensa, and H. cerberea, all successfully treated
with funnel-web spider antivenom.11.2 Internally extracted data on casesSee cases listed in 11.1. (Fisher et al 1980, 1981, 1989, Fisher
1989, DieckmanN et al 1989)11.3 Internal cases12. ADDITIONAL INFORMATION12.1 Availability of antidotes:Specific Funnel-web Spider Antivenom is available from the
manufacturer (or agents), Commonwealth Serum Laboratories, 45
Poplar Road, Parkville, Vic, 3052 AUSTRALIA. Current cost in
Australia, $491.00 per ampoule. Advice available from
manufacturer, telephone (03) 389 1911, telex AA 32789, Fax (03)
389 1434, International Fax +61 3 389 1434.12.2 Specific preventive measures:In areas known or likely to have funnel-web spiders, avoid
contact with spiders. Do not leave clothing or footwear on the
floor or where spiders may enter. Check gloves, footwear, and if
appropriate, clothing, for spiders prior to use. Use care when
working in areas where spiders may be common, such as in gardens,
rockeries, under materials left lying on the ground (clean them
up),and under houses. Do not place hands in places not visually
inspected first. Don't walk about at night bare-footed or
wearing 'thongs' or sandals. Attach draught strips to possible
under door entry points and flywire screens to windows and
ventilators. Check swimming pools, including filters, for
wandering spiders that sometimes fall in, as they can take many
hours to drown. If working or living in areas at risk from
funnel-web spiders, ensure appropriate first aid materials
available (bandages, splints) and methods understood by all those
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J. Arachnol., 8(3): 251-266.14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)Authors: Dr Julian White
State Toxinology Services
Adelaide Children's Hospital
North Adelaide SA 5006
Australia
Tel: 61-8-2047000
Mobile tel: 61-18-832776
Fax: 61-8-2046049
Dr Michael Gray
Head, Invertebrate Zoology
The Australian Museum
College Street
Sydney NSW 2000
Australia
Dr Malcolm Fisher
Head, Intensive Care Unit
The Royal North Shore Hospital of Sydney
Pacific Highway
St Leonards NSW 2065
Australia
Date: July 1989
Reviewer: Reviewed by Working Group on Natural Toxins November 1991